Abstract # 1761 Neonatal immune activation with lipopolysaccharide and a ‘second hit’ of adulthood stress alters ovarian inflammatory mediators: Implications for female subfertility

Abstract

Agnogentic subfertility is a clinical concern for many women of a healthy reproductive age. Accumulating evidence suggests developmental factors, such as immune status, are involved in the aetiology of female subfertility. Normal immune function is crucial for the initial quality and quantity of the ovarian follicular pool, and continued reproductive success. Our laboratory, in parallel with others, has established that early-life immune stress leads to sustained alterations in immune and neuroendocrine function, and perinatally programs vulnerability to subsequent stressors. However, investigation into the effects of early-life immune stress on female reproductive development is limited. This study investigates the immediate and long-term effects of immune activation during early-life on ovarian development and continued female reproductive health. Using a rat model, our findings suggest that neonatal immune activation (NIA) with lipopolysaccharide on post-natal days 3 and 5 leads to significant depletion of the ovarian follicular pool, acute upregulation of ovarian proinflammatory mediators, and precocious onset of puberty ( p p